The development of the kidneys and the efferent urinary tract is complex and unalterably interconnected. It is an essential part of embryonic development and closely connected to sexual development. Malformations lead to severe consequences and are often not compatible with postnatal life. In medical studies this is one of the most important themes in embryology.

00:00
We are going to putall this together now with RAAS and make sure
that you are truly familiar with the entireprocess of your RAAS system.
Lets begin. So here we are. I want youto begin at the kidney. Please begin at the
kidney and why would you want to release therenin? Decreased perfusion to the kidney.Okay good.
Give me some differentials. I've walked you throughrenal artery stenosis adequately. What about
congestive heart failure? Decreased perfusionto the kidney. In these cases, those juxtaglomerular
cells are going to release renin. Hence, takea look, please. Decreased blood pressure is
then going to release your renin. Here continueforward. I want you to make sure you clear
by this. You are going to be an MD. You aregoing to be a doctor, but that MD stands for
macula densa. Macula densa will decrease bloodpressure. Walk me through this. Initially
decrease of blood pressure, decreased perfusion,decreased GFR, where is our macula densa? Distal
convoluted tubule. What is the name of thatsensor? Macula densa. I showed you a picture
earlier. What is that macula densa sense?It senses the sodium or chloride right. So
therefore now with decreased blood pressure,what is it doing? It's not sensing as much.
So all of this is going to help contributeto increasing renin. One last thing, when
we have a decrease in blood pressure, canI ask you what branch of the autonomic nervous
has to come out? Good. Sympathetic. What kindof receptor on your JGA? Good. Beta-1. Once
again get another factor to help you stimulaterenin. Here comes out and here is not ogen.
Now I would like for you to take a look atthis suffix. I would like for you to understand
this concept ogen. Whatdoes that even mean? Trypsinogen, fibrinogen,
angiotensinogen so on and so forth. So theterm ogen means weak. Weak precursor right. Most
of your proteins come from where? The liver.
02:12
What is the most abundant protein in our bodies?
Albumin. Coming from where? Liver. Here isangiotensin, angiotensinogen coming from the
liver. What does that renin do? Cleave offthe ogen. There it goes. What do you have? angiotensin
I. Where is the angiotensin I headed to? Tothe lung. What's there? ACE. So here, ACE,
angiotensin converting enzyme, will takethe I and turn into the infamous angiotensin II.
Now lets plug in some pathologies. Are you ready?What if you had a patient that ends up having
too much renin? Autonomously. There was nodecrease in blood pressure as an in setting event.
And imaging study you ended up finding a tumour.
02:59
Where? In the juxtaglomerular apparatus. Wow! And
you ended up finding increased blood pressure.
03:05
So if you have increase in renin, increase
in aldosterone, you have secondary hypertension.
03:10
Are we clear? What is this called? Reninoma.
You understand the physio. You can easy putin the pathology and you see your patient.
You can actually see your patient. Next, giveme a pathology in which your ACE might be
elevated. A pathology. May be something likeWhat if I told you non-caseating granuloma,
bilateral hilar lymphadenopathy inan African-American female. You will tell
me? Good. Sarcoidosis. And sarcoidosis you couldhave increased production of ACE. What does
this mean? Increased production of angiotensin IINow with all that said lets say that
you give an ACE inhbitor. When you have anACE inhibitor, then you knock it out and you
can never form angiotensin II and never releaseyour aldosterone. Stop there for
one second.
03:56
The branch that is important for us, bradykinin.
ACE, angiotensin converting enzyme is an enzymethat you must know as being the enzyme responsible
for metabolism of bradykinin. Two major effectsof bradykinin that you would want to know as being
a side effect of what drug? ACE inhibitor.
04:18
A dry cough, And number 2, angioedema. So bradykinin,
increased capillary permeability. And number 2, Mightbe something like dry cough. And with that dry
cough, which is incredibly irritating youchange the drug into ARBs. Got it? Lets move on.
Angiotensin II vasoconstriction preferentially what partof the arteriole? Efferent.
What would it do to your blood vessels in general?It will cause contraction, vasoconstriction.
What are you are trying to do? Increased bloodpressure. What was in setting event. Take
a look, please. The first box, over ontoyour left is decreased blood pressure. You're
trying to increase your blood pressure. There ismy efferent arteriole. What does it do?
Do not memorize this. Close your eyes. Let meask you a question. Number one. You have
efferent arteriole vasoconstriction. Tell me about renal bloodflow when the plasma flow, decreased. Next
efferent arteriole vasoconstriction.
05:21
Tell me about GFR, Increased. Tell me the equation
for filtration fraction. GFR/renal plasma flow.
05:28
Good. You do the math. What do you get for
filtration fraction? Increased. Good move on.
05:36
What else happens? While angiotensin II
is going to go where, that's the organ, adrenal.
05:41
Which part? Cortex. What part of the cortex? and I am
going to keep pushing you here. What part of the cortex?Glomerulosa. Angiotensin II is going
to work on the glomerulosa to stimulate what'sknown as aldosterone synthase. Here comes
an aldosterone. Close your eyes. You knowthis from physio already. Aldosterone turns
to your collecting duct. Aldosterone workson your principal cells principally. What
does it do? It works on your sodium channelseverywhere. What do you mean everywhere? Well, principal cell.
You picturing that? Where am I? Collecting duct okay fineand it is facing whom? Urine. It is facing
the urine. So that is known as the apicalmembrane. That apical membrane has a sodium
channel. Aldosterone could work on that ENAC.
06:32
It is called Epithelial Sodium Channel. E,
epithelium; sodium channel, ENAC. Aldosteroneworks there to remove the sodium from the
urine. You know that already. Next, on thebasolateral membrane only, you have your sodium-
potassium ATPase pump. So what kind of effectdoes aldosterone have on your pump Tell me about that pump.
Sodium being kicked out. Kicked out intowhere? Into your blood. Aldosterone will stimulate
that pump. We have addressed this. Insertionin principal cells enhances stop there. So
you are going to reabsorb sodium. You are going totake out two. What do you mean take out? You
are going to literally remove and secretetwo substances into urine. First will be potassium,
next will be hydrogen. Okay. You can see. We are going towork through a lot of pathologies here, aren’t
we? Because you can have issues when you have too muchaldosterone, and you can have issues in which
you have two little aldosterone. Too muchaldosterone. Give me two differentials.Number 1
Conn exclusive aldosterone secreting tumour.
07:45
Cushing will be both cortisole and aldosterone.
Give me one aldosterone deficiency pathology,Addison. Addison's disease. So are these things
that we talked about? Of course keep repeating.
08:00
So when we have aldosterone it will reabsorb sodium.
It will kick out the potassium meaning tosay urinated out and it gets rid of your hydrogen.
So in Conn's syndrome tell me about the pHin that patient with Conn? Take your time.
Close your eyes. Reabsorbing too much sodium.
08:17
Getting rid of too much hydrogen. What happens
to your pH? Increases alkalosis in Conn. Confirmit. Why? Because you will find many patients
with secondary hypertension and Conn syndrome.
08:28
Many, not rare. Many.
08:32
Great favourable sodium gradient and along
with sodium what comes out? Fluid. Tell mewhat is it that contributes to the pitting edema
and congestive heart failure? The aldosterone.
08:44
Why? Because of this entire mechanism, we
just went through. Are we done? Not quiteyet because a decrease in blood pressure,
but there is another hormone that also comesinto play, and angiotensin II not only will
it be responsible for releasing that aldosteronefrom adrenal cortex, but angiotensin II also
works on the posterior pituitary. Why, why,why, why? Decreased blood pressure is what
the kidney is thinking? This angiotensin IIis then going to walk on the posterior pituitary
and so, therefore, you are going to releaseADH. Tell me about ADH, antidiuretic hormone.
That works on the, also collecting duct. What doesit do? It works through your V2 receptors.
How many kidneys do you have? I think one.
09:28
No no. Who? I think I have two. You have two
kidneys. So V2 receptors is what ADH workson. Gotta have fun with this just a little bit huh.
So works on V2 receptors and what does itdo? It is then going to insert aquaporins.
So that you do only what please, antidiuretichormone. What is another name for ADH? Vasopressin
and you are only going to reabsorb water,water, water in the hopes of doing what? In
the hopes of restoring osmolarity. In the hopesof restoring some of your blood pressure.
Now couple of important things about angiotensin IIin addition, is that it does work. Please
pay attention. That's its proximal convolutedtubule. Angiotensin II earlier through aldosterone.
May I ask you questions? Worked where? Collectingduct. Angiotensin II here is working on proximal
tubule. What does it do? It reabsorbs yoursodium. Don't memorize this. What are we doing?
There was a decrease in blood pressure asbeing the inciting event right. Now the angiotensin
II is going to work on your proximal convolutedtubule so you can try to remove more sodium
in exchange for hydrogen. So water reabsorptionand then can permit what is known as contraction
alkalosis and what that basically means isthat you are going to have contraction and
along with it you have also hydrogen leavingresulting in alkalosis.
10:58
Finally, in the hypothalamus, it has thirst.
Now all of this is then going to contributeto release of ADH. So ladies and gentleman
angiotensin II as you can see here from theorigin of it all with that initial event of
whatever it may be is causing decreased perfusionto the kidney. Once it gets into the renin
realm, now renin along with angiotensin IIand aldosterone my goodness gracious right
up and down the body has all kinds of incredibleeffects, and all these pathologies that we're
going to put in here including some of ourissues with ADH and diabetes insipidus right.
Central nephrogenic, we are going to bringall this into play, but if your foundation
isn't strong it is going to make it quitedifficult for me and you to work together
so that we can accomplish our goals effectively.

About the Lecture

The lecture Renin-Angiotensin-Aldosterone-System by Carlo Raj, MD is from the course Renal Diagnostics.

Included Quiz Questions

Which of the following statements about Conn’s syndrome is INCORRECT?

It results in excess cortisol.

It results in excess aldosterone.

It is a tumor of the adrenal gland.

It often presents with patients in alkalotic state.

It often presents with secondary hypertension.

Production of aldosterone involves multiple steps. Which step is CORRECTLY paired with its location?

All are correct.

Renin released from juxtaglomerular cells.

Angiotensin I is formed in the blood by renin stimulation.

Angiontensin converting enzyme in the lung forms angiotensin II.

Angiotensinogen formed in the liver.

Which of the following is NOT a direct action of angiotensin II?

Metabolism of bradykinin.

Stimulates ADH release from posterior pituitary.

Release of aldosterone from the zona glomerulosa

Stimulation of the hypothalamic thirst center.

Na+/H+ activity in the proximal convoluted tubule.

Which of the following is NOT a likely cause of secondary hypertension?

Addison’s disease.

Reninoma.

Cushing’s disease.

Renal artery stenosis.

Conn’s syndrome.

What pathology is associated with an increase in angiontensin converting enzyme activity?

Sarcoidosis

Addison’s disease

Angioedema.

Renal artery stenosis.

Tumor of the juxtaglomerular apparatus

Which of the following is NOT a direct effect of aldosterone release from the adrenal gland?

Decreases water reabsorption in the nephron.

ENac upregulation on the apical membrane in the collecting duct.

Increases sodium absorption overall.

Stimulates the Na/K+ pump on the basolateral membrane stimulating K+ release into the lumen..

Stimulates secretion of hydrogen ions in the collecting duct.

Author of lecture Renin-Angiotensin-Aldosterone-System

Carlo Raj, MD

Customer reviews

(3)
4,0 of 5 stars

5 Stars

2

4 Stars

0

3 Stars

0

2 Stars

1

1 Star

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Certainly one of the best explanations one could get on this topic!

By Mariia R. on 13. October 2018 for Renin-Angiotensin-Aldosterone-System

Amazing! I really get the material, Dr. Raj! I love how you keep reinforcing the material during each lecture!

Great presentation

By Lisa W. on 24. March 2018 for Renin-Angiotensin-Aldosterone-System

i like his fun attitude to teaching. It works for me!

Relax

By Tracey H. on 21. October 2017 for Renin-Angiotensin-Aldosterone-System

It would be nice if the material was presented in a less intense manner. It feels more like he is prepping football players for a big game. It is very distracting. Perhaps, if the lecture didn't feel so choppy it would be more enjoyable.

User Reviews

(3)
4,0 of 5 stars

5 Stars

2

4 Stars

0

3 Stars

0

2 Stars

1

1 Star

0

Certainly one of the best explanations one could get on this topic!

By Mariia R. on 13. October 2018 for Renin-Angiotensin-Aldosterone-System

Amazing! I really get the material, Dr. Raj! I love how you keep reinforcing the material during each lecture!

Great presentation

By Lisa W. on 24. March 2018 for Renin-Angiotensin-Aldosterone-System

i like his fun attitude to teaching. It works for me!

Relax

By Tracey H. on 21. October 2017 for Renin-Angiotensin-Aldosterone-System

It would be nice if the material was presented in a less intense manner. It feels more like he is prepping football players for a big game. It is very distracting. Perhaps, if the lecture didn't feel so choppy it would be more enjoyable.

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